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A. W. Musk. Department of Respiratory Medicine, Sir Charles Gairdner Hospital and School of Population Health, University of Western Australia, Nedlands, WA, Australia

Although asbestos has been used for various purposes since antiquity, asbestos related diseases did not begin to come to the notice of the medical profession until the turn of the 20th century. As industrialisation expanded, the value of asbestos as a cheap, strong, fire and acid resistant insulator was recognised. Records of cases of asbestosis date back to 1898, and Cooke first described asbestos as a cause of pulmonary fibrosis in the scientific medical literature in 1924. There was extensive evidence of an association between asbestos and lung and pleural cancer, particularly from Germany, in the 1930s, but it was not until 1955 that Richard Doll clearly demonstrated its causative relationship to lung cancer and Wagner its almost unique role in the causation of malignant mesothelioma in 1959. Industry (including the insurance industry), governments and trade unions were slow to respond effectively to the emerging information on the health effects of asbestos. Moreover, the deliberate suppression of important findings of asbestos industry sponsored research from the 1930s has also been documented. It has now been well shown that asbestos exposure may not only cause asbestosis, lung cancer, and malignant mesothelioma of the pleura and peritoneum, but also pleural plaques, diffuse/progressive pleural thickening, coarse fibrosis (crow’s feet), and rolled atelectasis of the lung, and possibly other cancers. Most of these diseases are dose related, but differ markedly in their relationships to time since first exposure to asbestos. The propensity of the various forms of asbestos to cause disease differs; for instance, for mesothelioma the relative potency of crocidolite:amosite:chrysotile is 500:100:1. There is a clear interaction of asbestos and tobacco smoking in determining the incidence of lung cancer. Recommendations for control of exposure of workers to asbestos were first introduced in Great Britain in 1906, and exposure standards were progressively adopted; in the USA in 1938 and Western Australia in 1951. However, workplaces did not comply in many industries (for example, the Wittenoom crocidolite industry and the transport industry) and as a result, an epidemic of asbestos related diseases has resulted and continues. Studies of exposure–response relationships have permitted predictions for the future incidence of disease; however, economic factors still prevail, thus in some countries asbestos (even crocidolite) is still mined and used. While animal studies have been helpful in determining the mechanisms of fibre carcinogenesis, epidemiology has been the pre-eminent scientific discipline for understanding the health effects of asbestos and crucial to the knowledge of asbestos related diseases. Epidemiologists have informed occupational health regulation, which has had a direct beneficial effect in improving the health of workers.


P. Gander. Sleep/Wake Research Centre, Massey University, Wellington, New Zealand

Some of the more radical French thinkers describe sleep as a revolutionary activity that should be used as a weapon against the evils of capitalism. Instead of striking, workers should have a nap, they say.

The Times, London, June 2004

Sleep can be thought of as a set of processes that the brain and body need to recover from the exertions of waking activity. In this sense, sleep is homeostatic, restoring the brain and body to an equilibrium for optimal waking function. Chronic sleep restriction and excessive sleepiness are commonplace among people of working age, and in particular among shiftworkers. For example, a recent national survey of New Zealanders aged 30–60 years (71% response rate) estimated that 37% report never or rarely getting enough sleep, and 15% experience excessive daytime sleepiness. A second survey of 20–60 year olds (72.5% response rate) found that night work, unemployment, and socioeconomic deprivation were significant independent predictors of reporting chronic sleeping problems, which affect an estimated 25% of people in this age range. It is well established that experimental sleep restriction across a series of nights causes cumulative degradation in performance and mood, and increases sleepiness and subjective fatigue. These predictable changes in human functional capacity translate into increased risk of occupational safety incidents and accidents. Recent experimental studies have also shown rapid effects of sleep restriction on carbohydrate metabolism, and on endocrine and immune function, leading to concerns that ongoing sleep restriction may facilitate the development of chronic conditions such as obesity, diabetes, and hypertension. Understanding the dynamics of sleep loss and recovery is vital to improving occupational health and safety. Innovative strategies are being developed to manage these issues at the legislative, industry, company, and individual level.